The beginning was the worst. It frustrated Janet Parkerson when her father started to forget what he had done that day or the day before.

But soon, names slipped his mind too, and then he failed to recognise people. Then he lost his ability to talk and to walk, and then he died, bedridden.

“I saw my father die of Alzheimer’s,” said Parkerson, 85. “I’ve experienced a lot of what it’s like – it’s terribly sad – and I would be very happy to help people not go through that.”

That’s why she decided to enroll in a five-year-long Alzheimer’s research study in 2014.

In fall 2018, she eagerly sat in the auditorium of East Ridge at Cutler Bay, her Pine Crest senior living community in Florida, United States, alongside about 50 other fellow residents, some of whom had also volunteered for the studies.

They were all there to hear from the man who recruited them for the study, Dr David Loewenstein, a University of Miami expert in neuropsychology who has been studying Alzheimer’s for 32 years.

Dr Loewenstein spoke about one of his team’s most recent findings: For the first time, they successfully used a behavioural test to identify which patients with cognitive impairment are most likely to develop Alzheimer’s.

He and his colleagues found patients with mild cognitive impairment, then divided them into three groups.

The first was patients with underlying Alzheimer’s, as proved by their high levels of amyloid, an aggregation of a protein in the brain of Alzheimer’s patients.

The second was patients who had the symptoms of Alzheimer’s, but didn’t have the high levels of amyloid, which meant they probably had another disease.

And the third included patients with other neurological conditions, such as depression.

Dr Loewenstein’s team used a cognitive stress test developed in 2013 by the University of Miami, and it involves researchers asking patients to learn a list of 15 words from three categories, five from each.

They then ask the patients to learn a new list of 15 words from the same categories.

Using the test, they found the patients with the high amyloid levels had the most trouble remembering the second list of words because the first interfered, even after the patients were given multiple attempts.

This means they accurately identified patients who actually have Alzheimer’s from those who look like they do, but don’t. “It’s a landmark finding,” said Dr Loewenstein.

When he finished his hour-long presentation at East Ridge on Oct 1, 2018, about 15 people rushed to talk to him. Most were fascinated by the fact some of them had had a part in the discovery.

Dr Loewenstein and his team have received more than US$10mil (RM41.4mil) in US state and federal funding for research in the last five years.

In June 2018, he was named the director of the Center for Cognitive Neuroscience and Aging at the University of Miami, which aims to tackle Alzheimer’s as it becomes a greater issue.

As more and more baby boomers get older, the number of Alzheimer’s patients is increasing.

Dr Loewenstein said if the disease isn’t stopped, in the next 10 to 15 years, it will wreak havoc for patients and their families, as well as bankrupt the US federal government, because the cost to care for the ill will be so high.

His team’s most recent milestone with the cognitive stress test helps researchers better understand Alzheimer’s and identify the earliest changes that take place in the brain because of it.

This test could potentially help doctors screen patients for Alzheimer’s at a much cheaper cost than through an amyloid PET scan.

The test will also help scientists better select candidates with Alzheimer’s for clinical and prevention trials.

“I’m satisfied with the effort,” Dr Loewenstein said. “We’re trying very hard, but I don’t think I’ll be completely satisfied until we have a cure or a prevention.

“We’re close, but we’re still not there.” – Miami Herald/Tribune News Service

RESEARCHERS may have found a tiny culprit – the human herpes virus – in the progressive loss of memory, thinking ability and identity that comes with Alzheimer’s disease. And it could be a big deal.

In research that revives a suspicion first raised more than six decades ago, scientists have found higher levels of the common virus in the brains of people who had both behavioural symptoms and neurological evidence of Alzheimer’s at the time of their death than in the brains of deceased donors who had no signs of dementia.

The researchers’ suspicions fell upon two strains of herpes virus — herpesvirus 6A and herpesvirus 7 — that were most evident in regions of the brain affected first in Alzheimer’s disease and in those that suffer most as the disease progresses.

Their surprise discovery emerged as researchers sorted through a vast genomic data bank in search of new ideas for treating Alzheimer’s with drugs designed for other diseases. The study’s authors pored over DNA and RNA sequencing data from 622 brains donated by people affected by Alzheimer’s and 322 brains that were free of the disease.

The data they mined is usually discarded, but was archived instead by the US National Institutes of Health in a bid to accelerate the discovery of new treatments by fostering “big data” collaborations.

This one brought together scientists at Arizona State University’s Banner Neurodegenerative Disease Research Center and Alzheimer’s experts at New York’s Icahn School of Medicine at Mount Sinai. It was published in the journal Neuron.

An estimated 5.7 million people in the US are living with Alzheimer’s disease in 2018, a number expected to rise to 14 million by 2050 unless some means of prevention or treatment is found.

The findings are a far cry from establishing what role the two strains of the virus might play in initiating or driving the decades-long process of cognitive loss and brain changes in Alzheimer’s, or even if they play such a causative role.

But it gives researchers a new foothold in a field of research that has failed to find anything to prevent, slow or reverse Alzheimer’s inexorable march.

“It is a beautiful piece of work, but it is still an association,” said Miroslaw Mackiewicz, programme director at the US National Institute on Aging’s Division of Neuroscience.

Still, he added, by providing evidence for the virus’ presence and some hints at its possible role, “you have some way to start your experiments”.

If further research uncovers a key role of herpes virus in Alzheimer’s disease, “this would generate a lot of excitement because we have vaccines” against various strains of disease-causing herpes virus, he said.

Dr Sam Gandy, an Alzheimer’s disease researcher at Icahn and one of the paper’s authors, said that if further research confirms that herpes virus is a predictable feature of Alzheimer’s disease, anti-viral treatments already in wide use might prove to be useful.

Dr Gandy cited research that identified high levels of retrovirus in the brains of patients with Amyotrophic Lateral Sclerosis (ALS, or Lou Gehrig’s Disease).

Even as researchers are still uncertain what role such viruses play in the disease, a clinical trial is underway to explore whether treatment with an anti-retroviral therapy used to treat HIV may affect the progression of ALS.

Herpes virus may not play a direct role in Alzheimer’s disease at all, the authors of the new research acknowledge.

There are many possible explanations for why herpes virus levels were so high in brains affected by Alzheimer’s. Among them: that Alzheimer’s might be an inflammatory or immune system reaction.

High levels of herpes virus might have touched off such a reaction, the authors of the new research note. Or the abundant presence of the virus could be an unrelated consequence of a brain struggling to defend itself from a different threat altogether.

Even if the abundance of herpes virus “is a secondary phenomenon, if it’s contributing to progression of Alzheimer’s, then treating it still could be beneficial”.

Finding and treating people with a known risk for Alzheimer’s and who have high viral loads might make a difference, he said.

Heather M. Snyder, senior director of medical and scientific operations for the Alzheimer’s Association, urged caution in interpreting the new findings.

“The idea that viruses or something else could be triggering or causing changes in the brain is not new,” she said.

“And we know that people in general, and those over 50 in particular, have these viruses in their brains. It might be more the immune system and that it may go awry. But we don’t know that.”

The new study not only “opens that door to asking those questions”, she said. It highlights a new way for such discoveries to be made.

“These findings came about because of researchers’ ability to share data, samples, funding and a large dataset,” she said. “That’s where increased funding continues to be so needed.”

As research teams run down the dynamics behind associations like this one, “it’s like an onion”, said Snyder. “We’re peeling back those layers and are getting to the core” of what causes Alzheimer’s disease and how to stop it. – Los Angeles Times/Tribune News Service

Jordan Michelle vapes a CBD oil made from hemp at the Cannabis World Congress Conference.

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Spencer Platt/Getty

States around the country – 29 of them, plus Washington DC – have legalized medical marijuana.

The American public largely supports the legalization of medical marijuana. At least 84% of the public believes the drug should be legal for medical uses, and recreational pot usage is less controversial than ever, with at least 61% of Americans in support.

Even though some medical benefits of smoking pot may be overstated by advocates of marijuana legalization, recent research has demonstrated that there are legitimate medical uses for marijuana and strong reasons to continue studying the drug’s medicinal uses.

Even the NIH’s National Institute on Drug Abuse lists medical uses for cannabis.

There are at least two active chemicals in marijuana that researchers think have medicinal applications. Those are cannabidiol (CBD) – which seems to impact the brain without a high- and tetrahydrocannabinol (THC) – which has pain relieving properties and is largely responsible for the high.

But scientists say that limitations on marijuana research mean we still have big questions about its medicinal properties. In addition to CBD and THC, there are another 400 or so chemical compounds, more than 60 of which are cannabinoids. Many of these could have medical uses. But without more research, we won’t know how to best make use of those compounds.

More research would also shed light on the risks of marijuana. Even if there are legitimate uses for medicinal marijuana, that doesn’t mean all use is harmless. Some research indicates that chronic, heavy users may have impaired memory, learning, and processing speed, especially if they started regularly using marijuana before age 16 or 17.

For some of the following medical benefits, there’s good evidence. For others, there’s reason to continue conducting research.

Jennifer Welsh contributed to an earlier version of this story.

The best-supported medicinal use of marijuana is as a treatment for chronic pain.

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A medical marijuana display.

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REUTERS/Jonathan Alcorn

A recent report by the National Academies of Sciences, Engineering, and Medicine said there was definitive evidence that cannabis or cannabinoids (which are found in the marijuana plant) can be an effective treatment for chronic pain.

The report said that is “by far the most common” reason people request medical marijuana.

There’s also strong evidence medical cannabis can help with muscle spasms.

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Medical marijuana is displayed in Los Angeles, California, U.S. August 6, 2007.

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REUTERS/Mario Anzuoni/File Photo

That same report said there’s equally strong evidence marijuana can help with muscle spasms related to multiple sclerosis.

Other types of muscle spasms respond to marijuana as well. People use medical marijuana to treat diaphragm spasms that are untreatable by other, prescribed medications.

It doesn’t seem to harm lung capacity, and may even improve it.

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Christopher Furlong/Getty Images

There’s a fair amount of evidence that marijuana does no harm to the lungs, unless you also smoke tobacco. One study published in Journal of the American Medical Association found that not only does marijuana not impair lung function, it may even increase lung capacity.

Researchers looking for risk factors of heart disease tested the lung function of 5,115 young adults over the course of 20 years. Tobacco smokers lost lung function over time, but pot users actually showed an increase in lung capacity.

It’s possible that the increased lung capacity may be due to taking a deep breaths while inhaling the drug and not from a therapeutic chemical in the drug.

The smokers in that study only toked up a few times a month, but a more recent survey of people who smoked pot daily for up to 20 years found no evidence that smoking pot harmed their lungs, either.

The National Academies report said there are good studies showing marijuana users are not more likely to have cancers associated with smoking.

It may be of some use in treating glaucoma, or it may be possible to derive a drug from marijuana for this use.

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thematthewknot via Flickr

One of the most common reasons that states allow medical marijuana use is to treat and prevent the eye disease glaucoma, which increases pressure in the eyeball, damaging the optic nerve and causing loss of vision.

Marijuana decreases the pressure inside the eye, according to the National Eye Institute: “Studies in the early 1970s showed that marijuana, when smoked, lowered intraocular pressure (IOP) in people with normal pressure and those with glaucoma.”

For now, the medical consensus is that marijuana only lowers IOP for a few hours, meaning there’s not good evidence for it as a long term treatment right now. Researchers hope that perhaps a marijuana-based compound could be developed that lasts longer.

It may help control epileptic seizures.

Some studies have shown that cannabidiol (CBD), another major marijuana compound, seems to help people with treatment-resistant epilepsy.

A number of individuals have reported that marijuana is the only thing that helps control their or their children’s seizures.

However, there haven’t been many gold-standard, double-blind studies on the topic, so researchers say more data is needed before we know how effective marijuana is.

It also decreases the symptoms of a severe seizure disorder known as Dravet’s Syndrome.

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Charlotte Figi has Dravet’s Syndrome, and her parents are giving her marijuana to treat her seizures.

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CNN/WEED

During the research for his documentary “Weed,” Sanjay Gupta interviewed the Figi family, who treated their 5-year-old daughter using a medical marijuana strain high in cannabidiol and low in THC.

According to the film, the drug decreased her seizures from 300 a week to just one every seven days. Forty other children in the state were using the same strain of marijuana to treat their seizures when the film was made – and it seemed to be working.

The doctors who recommended this treatment said the cannabidiol in the plant interacts with brain cells to quiet the excessive activity in the brain that causes these seizures.

Gupta notes, however, that a Florida hospital that specializes in the disorder, the American Academy of Pediatrics, and the Drug Enforcement agency don’t endorse marijuana as a treatment for Dravet or other seizure disorders.

A chemical found in marijuana stops cancer from spreading, at least in cell cultures.

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crafty_dame via flickr

CBD may help prevent cancer from spreading, researchers at California Pacific Medical Center in San Francisco reported in 2007.

Other very preliminary studies on aggressive brain tumors in mice or cell cultures have shown that THC and CBD can slow or shrink tumors at the right dose, which is a strong reason to do more research.

One 2014 study found that marijuana can significantly slow the growth of the type of brain tumor associated with 80% of malignant brain cancer in people.

Still, these findings in cell cultures and animals don’t necessarily mean the effect will translate to people – far more investigation is needed.

It may decrease anxiety in low doses.

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KieferPix/Shutterstock

Researchers know that many cannabis users consume marijuana to relax, but also that many people say smoking too much can cause anxiety. So scientists conducted a study to find the “Goldilocks” zone: the right amount of marijuana to calm people.

According to Emma Childs, an associate professor of psychiatry at the University of Illinois at Chicago and an author of the study, “we found that THC at low doses reduced stress, while higher doses had the opposite effect.”

A few puffs was enough to help study participants relax, but a few puffs more started to amp up anxiety. However, people may react differently in different situations.

THC may slow the progression of Alzheimer’s disease.

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REUTERS/Brian Snyder

Marijuana may be able to slow the progression of Alzheimer’s disease, a study led by Kim Janda of the Scripps Research Institute suggests.

The 2006 study, published in the journal Molecular Pharmaceutics, found that THC (the active chemical in marijuana) slows the formation of amyloid plaques by blocking the enzyme in the brain that makes them. These plaques kill brain cells and are associated with Alzheimer’s.

A synthetic mixture of CBD and THC seems to preserve memory in a mouse model of Alzheimer’s disease. Another study suggested that a THC-based prescription drug called dronabinol was able to reduce behavioral disturbances in dementia patients.

All these studies are in very early stages, though, so more research is needed.

The drug eases the pain of multiple sclerosis.

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Customers shop for “Green Friday” deals at the Grass Station marijuana shop on Black Friday in Denver

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Thomson Reuters

Marijuana may ease painful symptoms of multiple sclerosis, according to a study published in the Canadian Medical Association Journal.

Jody Corey-Bloom studied 30 multiple sclerosis patients with painful contractions in their muscles. These patients didn’t respond to other treatments, but after smoking marijuana for a few days, they reported that they were in less pain.

The THC in marijuana seems to bind to receptors in the nerves and muscles to relieve pain.

It seems to lessen side effects from treating hepatitis C and increase treatment effectiveness.

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Reuters

Treatment for hepatitis C infection is harsh: negative side effects include fatigue, nausea, muscle aches, loss of appetite, and depression. Those side effects can last for months, and lead many people to stop their treatment course early.

But a 2006 study in the European Journal of Gastroenterology and Hepatology found that 86% of patients using marijuana successfully completed their Hep C therapy. Only 29% of non-smokers completed their treatment, possibly because the marijuana helps lessen the treatment’s side effects.

Marijuana also seems to improve the treatment’s effectiveness: 54% of hep C patients smoking marijuana got their viral levels low and kept them low, in comparison to only 8% of nonsmokers.

Marijuana may help with inflammatory bowel diseases.

University of Nottingham researchers found in 2010 that chemicals in marijuana, including THC and cannabidiol, interact with cells in the body that play an important role in gut function and immune responses. The study was published in the Journal of Pharmacology and Experimental Therapeutics.

The body makes THC-like compounds that increase the permeability of the intestines, allowing bacteria in. But the cannabinoids in marijuana block these compounds, making the intestinal cells bond together tighter and become less permeable.

But the National Academies report said there isn’t enough evidence to be sure whether marijuana really helps with these conditions, so more research is needed.

It relieves arthritis discomfort.

Marijuana alleviates pain, reduces inflammation, and promotes sleep, which may help relieve pain and discomfort for people with rheumatoid arthritis, researchers announced in 2011.

Researchers from rheumatology units at several hospitals gave their patients Sativex, a cannabinoid-based pain-relieving medicine. After a two-week period, people on Sativex had a significant reduction in pain and improved sleep quality compared to placebo users.

Other studies have found that plant-derived cannabinoids and inhaled marijuana can decrease arthritis pain, according to the National Academies report.

Marijuana users tend to be less obese and have a better response to eating sugar.

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Flickr

A study published in the American Journal Of Medicine suggested that pot smokers are skinnier than the average person and have healthier metabolism and reaction to sugars, even though they do end up eating more calories.

The study analyzed data from more than 4,500 adult Americans – 579 of whom were current marijuana smokers, meaning they had smoked in the last month. About 2,000 people had used marijuana in the past, while another 2,000 had never used the drug.

The researchers studied how the participants’ bodies responded to eating sugars. They measured blood-sugar levels and the hormone insulin after participants hadn’t eaten in nine hours, and after they’d eaten sugar.

Not only were pot users thinner, their bodies also had a healthier response to sugar. Of course, the study couldn’t determine whether the marijuana users were like this to begin with or if these characteristics were somehow related to their smoking.

While not really a health or medical benefit, marijuana could spur creativity.

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Getty Images / Marc Piscotty

Contrary to stoner stereotypes, marijuana usage has actually been shown to have some positive mental effects, particularly in terms of increasing creativity, at least in some contexts. Even though people’s short-term memories tend to function worse when they’re high, they actually get better at tests requiring them to come up with new ideas.

Researchers have also found that some study participants improve their “verbal fluency,” their ability to come up with different words, while using marijuana.

Part of this increased creative ability may come from the release of dopamine in the brain, which lowers inhibitions and allows people to feel more relaxed, giving the brain the ability to perceive things differently.

Cannabis soothes tremors for people with Parkinson’s disease.

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Walter Hickey / BI

Research from Israel shows that smoking marijuana significantly reduces pain and tremors and improves sleep for Parkinson’s disease patients. Particularly impressive was the improved fine motor skills among patients.

Medical marijuana is legal in Israel for multiple conditions, and a lot of research into the medical uses of cannabis is done there, supported by the Israeli government.

Marijuana may help veterans suffering from PTSD.

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Walter Hickey / BI

In 2014, the Colorado Department of Public Health awarded $2 million to the Multidisciplinary Association for Psychedelic Studies (one of the biggest proponents of marijuana research) to study marijuana’s potential for people with post-traumatic stress disorder.

Naturally occurring cannabinoids, similar to THC, help regulate the system that causes fear and anxiety in the body and brain.

Marijuana is approved to treat PTSD in some states already – in New Mexico, PTSD is the number one reason for people to get a license for medical marijuana.

But there are still questions about the safety of using marijuana while suffering from PTSD, which this study – which has taken a while to get off the ground – will hopefully help answer.

Animal studies suggest that marijuana may protect the brain after a stroke.

Research from the University of Nottingham shows that marijuana may help protect the brain from damage from a stroke by reducing the size of the area affected by the stroke – at least in rats, mice, and monkeys.

This isn’t the only research that has shown neuroprotective effects of cannabis. Some research shows that the plant may help protect the brain after other types of brain trauma.

Marijuana might even protect the brain from concussions and trauma.

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Al Bello/Getty Images

Lester Grinspoon , a professor of psychiatry at Harvard and marijuana advocate, recently wrote an open letter to NFL Commissioner Roger Goodell. In it, he said the NFL should stop testing players for marijuana, and that the league should start funding research into the plant’s ability to protect the brain instead.

“Already, many doctors and researchers believe that marijuana has incredibly powerful neuroprotective properties, an understanding based on both laboratory and clinical data,” Grinspoon wrote.

Goodell said he’d consider permitting athletes to use marijuana if medical research shows that it’s an effective neuroprotective agent.

At least one recent study on the topic found that patients who had used marijuana were less likely to die from traumatic brain injuries.

It can help eliminate nightmares.

This is a complicated one, because it involves effects that can be both positive and negative. Marijuana disturbs sleep cycles by interrupting the later stages of REM sleep. In the long run, this could be a problem for frequent users.

However, for people suffering from serious nightmares, especially those associated with PTSD, this can be helpful, perhaps in the short term. Nightmares and other dreams occur during those same stages of sleep. By interrupting REM sleep, many of those dreams may not occur. Research into using a synthetic cannabinoid – similar to THC but not the same – showed a significant decrease in the number of nightmares in patients with PTSD.

Additionally, even if frequent use can be bad for sleep, marijuana may be a better sleep aid than some other substances that people use. Some of those, including medication and alcohol, may potentially have worse effects on sleep, though more research is needed on the topic.

Cannabis reduces some of the pain and nausea from chemotherapy and stimulates appetite.

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Harrison Jacobs/Business Insider

One of the most well-known medical uses of marijuana is for people going through chemotherapy. There’s good evidence that it’s effective for this, according to the National Academies report.

Cancer patients being treated with chemo suffer from painful nausea, vomiting, and loss of appetite. This can cause additional health complications.

Marijuana can help reduce these side effects, alleviating pain, decreasing nausea, and stimulating the appetite. There are also multiple FDA-approved cannabinoid drugs that use THC, the main active chemical in marijuana, for the same purpose.

Marijuana can help people who are trying to cut back on drinking.

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Thomson Reuters

Marijuana is safer than alcohol. That’s not to say it’s risk-free, but cannabis is much less addictive than alcohol and doesn’t cause nearly as much physical damage.

Disorders like alcoholism involve disruptions in the endocannabinoid system. Because of that, some people think cannabis might help patients struggling with those disorders.

Research published in the Harm Reduction Journal found that some people use marijuana as a less harmful substitute for alcohol, prescription drugs, and other illegal drugs. Some of the most common reasons patients make that substitution are that marijuana has less negative side effects and is less likely to cause withdrawal problems.

Some people do become psychologically dependent on marijuana, and it is not a cure for substance abuse problems. But from a harm-reduction standpoint, it can help.

Still, it’s worth noting that combining marijuana and alcohol can be dangerous, and some researchers are concerned that this scenario is more likely than one in which users substitute a toke for a drink.

While there are a number of factors behind the current opioid epidemic, many experts agree that the use of opioid painkillers to treat chronic pain has played a major role. It’s very risky to take powerful drugs that have a high risk of causing overdose and high addiction rates. Marijuana, which can also treat chronic pain, is far less risky.

Several studies have showed that states that allow medical marijuana have fewer opioid deaths. This effect seems to grow over time, with states who pass these laws seeing a “20% lower rate of opioid deaths in the laws’ first year, 24% in the third, and 33% in the sixth,” according to Stat News.

It’s hard to say that deaths went down because of medical marijuana legalization and not other reasons. But because the effect seems to get stronger the longer marijuana remains legal, researchers think marijuana is a likely cause of the decline in opioid deaths.

A FITFUL night’s sleep and a habit of daytime catnapping may be an early-warning sign of Alzheimer’s dementia, according to new research conducted in humans and mice.

Restless nights and sleepy days are a common pattern in patients with full-blown Alzheimer’s. Those disrupted circadian rhythms are a symptom that can upend the lives of caregivers and cause confusion and anxiety in patients.

Less dramatic levels of sleep disruption, including trouble falling asleep and more frequent night-time wakening, are also typical as people age.

A new study finds that, in older people who show no signs of cognitive impairment, those with a sleep-wake cycle that is subtly off-kilter are more likely to have amyloid protein deposits in their brains.

Those amyloid “plaques” are a hallmark of Alzheimer’s, and they can develop years before symptoms of memory loss or thinking problems are evident.

Study participants whose sleep patterns followed a clearer pattern of sleeping through the night and staying awake during the day were less likely to have significant clumps of amyloid protein in their brains, suggesting they were less likely to go on to develop Alzheimer’s disease.

The new research, published recently by the journal JAMA Neurology, doesn’t answer the question of whether a messy sleep pattern actually contributes to the development of Alzheimer’s or is just a sign of the disorder.

If it’s merely a sign of impending Alzheimer’s, it could still be a useful tell.

Currently, the earliest clear signs of Alzheimer’s disease – those plaque deposits – can only be detected with sophisticated brain imaging.

If physicians and researchers had a behavioural signpost that could be readily detected with a wearable activity monitor, they’d likely identify more people who could enroll in research studies, or who might benefit from early efforts to head off dementia.

On the other hand, if a sleep-wake cycle with frequent night-time awakening and more daytime sleeping actually helps Alzheimer’s gain a foothold, that finding could be even more valuable: Patients with broken sleep patterns could be counseled to take steps to improve their night-time sleep quality, perhaps delaying or preventing their progression toward dementia.

“I don’t want to scare people into thinking that if they wake up often at night they’ll have Alzheimer’s,” said study co-author Dr Erik S. Musiek, a Washington University neurologist who studies the role of the circadian clock on ageing.

Some changes in sleep are typical as people age. But while disrupted sleep patterns generally manifest themselves as night-time awakenings and short bursts of compensating daytime sleep, participants didn’t always notice or report these occurrences, Musiek said.

“These are subtle things, and we can detect them in a large group of people,” he said.

The role that sleep disruption plays in early Alzheimer’s – whether it contributes to the disease or merely signals its presence – should become clearer as his research team tracks study participants into old age.

In the meantime, research conducted on mice offers a tantalising peek at an answer, Musiek said.

When scientists from Washington University and the University of Pennsylvania bred mice whose normal circadian rhythms were completely knocked out by a combination of drugs and genetic engineering, amyloid plaques accumulated quickly in the hippocampus, a key structure in memory and learning.

Only later would the behavioural symptoms of Alzheimer’s appear.

That study, slated for publication in the Journal of Experimental Medicine, suggests that irregularities of circadian rhythm accelerate amyloid plaque accumulation in the brain and speed the appearance of Alzheimer’s more obvious symptoms – memory and thinking problems.

Whether that dynamic is repeated in humans remains to be shown.

In the research published recently, 189 participants had an average age of close to 67 years when they enrolled in the study between 2010 and 2012. Each wore an activity monitor for seven to 14 days.

The wearable device detected when and for how long a participant slept, how often she awakened at night, and when she appeared to be napping during the day.

The participants, both men and women, all were cognitively healthy at the time they enrolled, with no signs of mental impairment or memory problems.

Around the time they wore their activity devices, 142 of the participants also had a specialised PET scan of the brain to detect amyloid deposits.

Some 26 of the study’s subjects showed amyloid deposits suggestive of very early Alzheimer’s disease, while 116 did not.

On three of eight arcane measures of circadian function, the group with early Alzheimer’s scored higher than those shown to have no significant build-up of amyloid in their brains.

“A clear implication of our findings is that therapies directly targeting the circadian system to normalise circadian timing, rather than just augmenting total sleep, may be beneficial in the prevention of Alzheimer’s disease,” the authors wrote.

Musiek said he recommends a range of practices to patients concerned about the prospect of dementia.

They aren’t that different from the usual “sleep hygiene” practices that sleep-medicine specialists recommend for all patients.

“You want to consolidate your sleep as much as possible at night,” he said. “I always tell my patients not to use electronic devices at night, to sleep in a dark room — and to go to sleep, not watch TV in bed.”

Musiek also urges his patients to “get up in morning, get active, go out and get into the morning light”.

Eating a good breakfast “helps synchronise your clock”, he added.

Finally, he said, our early-bird and night-owl inclinations often have their roots in our genes. We would do well to try to accommodate, not fight, those differences.

“People get into trouble trying to force themselves into a different mode,” Musiek said. “We should listen to our bodies, and try to understand our own rhythms, and keep day and night within that range.” – Los Angeles Times/Tribune News Service

Me, submitting a sample of my spit for a DNA test. I didn’t have to submit new saliva to get the updated results.

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Hollis Johnson

Back in 2015, I decided to send my spit to 23andMe, the company that sells direct-to-consumer genetics tests.

The test gave me information as varied as how much DNA I share with our Neanderthal ancestors, how much caffeine I most likely consume, and whether I may have a unibrow. It also let me know whether I’m carrying certain genetic variations related to diseases that could be passed on to kids.

In April of last year, the US Food and Drug Administration told 23andMe it could start providing reports revealing whether you have certain risk factors for developing diseases including Parkinson’s disease and Alzheimer’s disease.

A year later, the FDA gave 23andMe clearance to tell consumers about their risk of cancer – specifically about three BRCA1 and BRCA2 gene mutations that are associated with an increased risk in breast and ovarian cancer. The test has genetic counselors and scientists concerned, because there are thousands of mutations associated with the BRCA1 and BRCA2 genes and this test screens for only three of them most commonly found in people of Ashkenazi (Eastern European) Jewish descent.

The version of the test that includes the health reports costs $199, while the ancestry test alone is $99. Here’s what it was like:

I first received my 23andMe test in 2015. Because I had already submitted my sample, I didn’t have to repeat the process to get my reports on health risks in 2017 or on BRCA mutations in 2018.

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Lydia Ramsey/Business Insider

That meant I didn’t have to resubmit a sample of my saliva, which was convenient. Spitting into the tube had taken me about five minutes the first time around.

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Lydia Ramsey/Business Insider

Before I shipped my spit, I registered online. I also got to decide whether I wanted to have my DNA used to research treatments for diseases. In the spirit of science, I decided to consent and sign the form.

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Lydia Ramsey/Business Insider

When I got my original report in 2015, I had 62 reports waiting for me based on my 23 pairs of chromosomes from mom and dad. The reports covered everything from family history to physical traits and genetic variants related to diseases that I could pass down to my kids.

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Lydia Ramsey/Business Insider

When I logged in to my 23andMe account in 2018, I was surprised to see that the number had increased to 81 (this is including the genetic-health-risk tests I opted into).

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23andMe

The new reports are available only to 23andme customers who had tests done on the company’s newest genotyping chip. That’s the vast majority of customers who were tested by late November 2013, according to a 23andme spokesman.

Of course, I still had the basics, such as my ancestry breakdown. This time, my results were even more specific, breaking down my Scandinavian ancestry into my Norwegian heritage specifically.

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23andMe

Learn more about ancestry tests.

Notably, more wellness reports were available than was the case when I most recently checked. In 2015, I spent time investigating my muscle composition, which told me I wasn’t a sprinter.

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Lydia Ramsey/Business Insider

Now, however, there were reports about my sleeping and eating habits. When it came to the genetics behind my weight, my results weren’t entirely unexpected — I had gotten the same results from another DNA test I took.

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23andMe

Review of Pathway Genomics Fit test.

Back when I first took the test, the most controversial part was the carrier-status test, which tells me whether I carry a variant that could be passed down to my children, resulting in a genetic disease. These were the tests the FDA needed to approve. 23andMe was very thorough in its presentation here, making it clear that the tests couldn’t be used to inform my own health.

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Lydia Ramsey/Business Insider

But in 2017, I had access to my genetic health risks, which could tell me whether I personally had an increased risk of getting certain diseases, including Parkinson’s and Alzheimer’s. My heart pounding, I clicked on a link that took me to the reports. Not everyone has to get the test. If you’re not ready, you can select “ask me again later,” and if you really never want to see the results, you can opt out entirely.

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23andMe

You can also choose to opt out of just the Alzheimer’s and Parkinson’s reports. Because the two neurodegenerative diseases have few treatments, getting the report could cause more anxiety than necessary.

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23andMe

On these two, I opted to defer. I made the decision after speaking with representatives from patient groups in 2017, who clarified what the reports could tell me and what I might want to do before looking at them.

For both Parkinson’s and Alzheimer’s, age is a bigger risk factor than genetics. With Parkinson’s, if I had a variant related to the disease, my risk of getting the disease would certainly be increased, but not by much.

Keith Fargo, the Alzheimer’s Association director of scientific programs and outreach, told Business Insider in 2017 that the Alzheimer’s report, which would tell me whether I had a mutation on my APOE gene, was more useful in the context of research than it was for predicting who might get the disease. And as I mentioned, I had allowed 23andMe to use my DNA for research purposes, so it was already getting put to use.

I also kept in mind my family history of one of these diseases. If I decide to view my results, I will plan on speaking with a genetic counselor before proceeding.

Another factor I noted was life insurance, something 23andMe’s report brings up as well. While genetic testing can’t prevent you from getting health insurance, life-insurance policies can use the information to deny your application. Since my results won’t be changing, I decided it would make the most sense to wait to get the results until I get life insurance. As long as I don’t know, there shouldn’t be a way for life insurers to find out.

Had I decided to see my results, 23andMe would have asked once more whether I was sure. This would have spelled out what exactly the risk window would be. If I had the highest risk, I’d have a 60% chance of developing Alzheimer’s by 85. Right now, roughly one-third of people over 85 have Alzheimer’s.

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23andMe

Had I chosen to see my Alzheimer’s results, they may look like this.

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23andMe

When I logged back in in 2018, I saw that there were now three health reports to choose from. Because I had fairly good reason to believe that I wouldn’t have one of the three variants, I decided it wouldn’t be a big deal to click through and see my results for that test.

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23andMe

When I spoke with a genetic counselor about this, she told me her bigger concern was that if someone of Scandinavian descent (like me) tested negative but did have a family history of breast and ovarian cancer, the person may not fully understand that he or she still could have a mutation, just not in the three tested. So I paid close attention to a paragraph explaining that the results of the report didn’t mean my risk of cancer was reduced.

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23andMe

Read more about the concerns over 23andMe’s cancer genetics test.

Cancer is a complex condition, and it can be caused by numerous factors — genetics being just one part of that. Should I have a mutation on BRCA1 or BRCA2 (identified by this test or elsewhere), the presence of a mutation doesn’t necessarily mean I have cancer, just that the chances are higher. For example, in the US, the average woman has a 7% of chance of getting breast cancer by age 70. That escalates to 50% if the woman has a mutation to her BRCA1 or BRCA2 genes. As part of my BRCA tutorial, 23andMe explained how different factors increase cancer risk.

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23andMe

Source: CDC

Further down the page on my BRCA results, there are resources for how to communicate the information to family members and physicians and how to get in touch with a genetic counselor.

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23andMe

Here’s a resource for finding a genetic counselor.

Afterward, I checked out my other genetic-health-risk reports. My results for Alpha-1 antitrypsin deficiency and celiac disease showed up on the same page as my BRCA results. On this page, I could also revisit whether I wanted to see my Parkinson’s or Alzheimer’s results.

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23andMe

The takeaway: It was fascinating to pop back in to my account and see new reports. I feel grateful that I don’t have to see my Parkinson’s disease and Alzheimer’s disease results, but I can still choose to check out my BRCA results — albeit with the big caveat that they’re likely to be negative anyway. Either way, it was fun to check in on my Neanderthal results.